ReviewJournal of inflammation research2025
The Interplay of Aging and PANoptosis in Osteoarthritis Pathogenesis: Implications for Novel Therapeutic Strategies.
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Epigenetic-metabolic coupling by SOX3/WDR5-SIRT5 signaling mediates the therapeutic effects of TGFβ-targeted exosomal nanoparticles in osteoarthritis.Materials today. Bio · 2026Article
- Article
- Isoquercitrin ameliorates chondrocyte dysfunction in osteoarthritis by targeting AKT1-mediated mitochondrial dynamics regulation.PloS one · 2026Article
- Paradigm shift in macrophage polarization in osteoarthritis: from M1/M2 imbalance to macrophage state reprogramming in the ageing immune microenvironment.Frontiers in immunology · 2026Review
- Inflammaging and immunosenescence-driven remodeling of the immune microenvironment in osteoarthritis: mechanisms, immune regulation and immune reprogramming.Frontiers in immunology · 2026Review
- Focus on necroptosis: its role in the pathogenesis and therapeutic potential of osteoarthritis.Frontiers in immunology · 2026Review
- Research progress on the role of CD14 in osteoarthritis.Frontiers in immunology · 2026Review
- RIPK1-targeted therapy alleviates intervertebral disc degeneration via inhibiting nucleus pulposus PANoptosis.Apoptosis : an international journal on programmed cell death · 2025Article
- Association between the C-reactive protein-albumin-lymphocyte (CALLY) index and osteoarthritis prevalence: a cross-sectional study of American adults based on NHANES.Frontiers in nutrition · 2025Article
- Role of Pyroptosis in the Pathogenesis of Osteoarthritis: An Updated Review.Journal of inflammation research · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a common degenerative joint disease characterized by the progressive degradation of articular cartilage, synovial inflammation, and subchondral bone remodeling. This review explores the interplay between aging, PANoptosis, and inflammation in OA progression. Age-related cellular and immune dysfunctions, including cellular senescence, senescence-associated secretory phenotypes (SASPs), and immunosenescence, significantly contribute to joint degeneration. In OA, dysregulated apoptosis, necroptosis, and pyroptosis, particularly in chondrocytes, exacerbate cartilage damage. Apoptosis, mediated by the JNK pathway, reduces chondrocyte density, while necroptosis and pyroptosis, involving RIPK-1/RIPK-3 and the NLRP3 inflammasome, respectively, amplify inflammation and cartilage destruction. Inflammatory cytokines and damage-associated molecular patterns (DAMPs) further enhance these PANoptotic pathways. Current therapeutic strategies primarily focus on anti-inflammatory agents such as non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids, with growing interest in anti-senescence drugs targeting cellular senescence and SASP. Additionally, exploring PANoptosis mechanisms offers potential for innovative OA treatments.
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